Journal
FRONTIERS IN CHEMISTRY
Volume 4, Issue -, Pages -Publisher
FRONTIERS MEDIA SA
DOI: 10.3389/fchem.2016.00021
Keywords
L1; retrotransposon; hepatitis C virus (HCV); hepatitis B virus (HBV); hepatocellular carcinoma
Categories
Funding
- KAKENHI from Japan Society for the Promotion of Science (JSPS) [15K08496]
- Takeda Science Foundation
- Senri Life Science Foundation
- Suzuken Memorial Foundation
- Shimizu Foundation for Immunology and Neuroscience
- NOVARTIS Foundation (Japan) for the Promotion of Science
- Grants-in-Aid for Scientific Research [15K08496] Funding Source: KAKEN
Ask authors/readers for more resources
Hepatocellular carcinoma (HCC) accounts for approximately 80% of liver cancers, the third most frequent cause of cancer mortality. The most prevalent risk factors for HCC are infections by hepatitis B or hepatitis C virus. Findings suggest that hepatitis virus-related HCC might be a cancer in which LINE-1 retrotransposon, often termed L1, activity plays a potential role. Firstly, hepatitis viruses can suppress host defense factors that also control L1 mobilization. Secondly, many recent studies also have indicated that hypomethylation of L1 affects the prognosis of HCC patients. Thirdly, endogenous L1 retrotransposition was demonstrated to activate oncogenic pathways in HCC. Fourthly, several L1 chimeric transcripts with host or viral genes are found in hepatitis virus-related HCC. Such lines of evidence suggest a linkage between L1 retrotransposons and hepatitis virus-related HCC. Here, I briefly summarize current understandings of the association between hepatitis virus-related HCC and L1. Then, I discuss potential mechanisms of how hepatitis viruses drive the development of HCC via L1 retrotransposons. An increased understanding of the contribution of L1 to hepatitis virus-related HCC may provide unique insights related to the development of novel therapeutics for this disease.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available